During the first quarter of the 21st century, iodized salt became available almost everywhere, and only isolated pockets of iodine deficiency remain in the world. By 2024, 126 countries had introduced mandatory iodine fortification of salt, 89% of the world’s population consumes iodized salt, and 101 countries have achieved adequate iodine status among their populations, whereas in 1993, low iodine intake was observed in 113 countries. This is why iodine fortification of salt is recognized as one of the greatest achievements in public health. The new recommendations reviewed in this paper update existing guidelines regulating salt fortification programs, their monitoring and evaluation, and propose using new approaches in combination with maintaining and strengthening measures that have proven effective and sustainable. Of the six "analytical notes" included in the guidelines, the section on improving the availability of data on the iodine status of the population may be of greatest interest to readers. According to the authors, the effectiveness of salt iodization programs should be assessed by integrating iodine status surveys into more comprehensive health and nutrition surveys of the population or through sentinel epidemiological monitoring in areas at high risk of iodine deficiency. Collecting urine samples in antenatal clinics during routine visits by pregnant women is likely to be a less resource-intensive approach than representative cross-sectional surveys of iodine status.

RELEVANCE. Primary hyperparathyroidism is one of the most common endocrine diseases characterized by impaired calcium-phosphorus metabolism due to hypersecretion of parathyroid hormone.

GOAL. Assessment of the epidemiological situation with parathyroid gland diseases in the Chuvash Republic based on data from the All-Russian Registry of Patients with primary hyperparathyroidism. To analyze the data of patients with primary hyperparathyroidism in a retrospective cohort study from 2014 to 2025 at the clinical base of the Republican Clinical Hospital for War Veterans of the Ministry of Health of Chuvashia.

MATERIALS AND METHODS. The data on the Chuvash Republic from the All-Russian Registry of patients with primary hyperparathyroidism are analyzed. In the course of a retrospective cohort study (2014–2025), a cohort of patients registered at the Republican Clinical Hospital for War Veterans of the Ministry of Health of Chuvashia was analyzed. For statistical data processing, a descriptive method was used with the calculation of absolute and relative values (percentages).

RESULTS. It was found that the prevalence of parathyroid gland pathology in the region is 73.4 cases per 100,000 population. Key epidemiological features were identified: a pronounced predominance of women (88.9%) in the older age group, an uneven geographical distribution with a concentration of cases in urbanized areas (Cheboksary, Novocheboksarsk), as well as a significant increase in detection in recent years. The data obtained indicate the influence of both organizational factors (availability of specialized care) and possible environmental risks (imbalance of trace elements in water sources) on the prevalence of pathology.

CONCLUSION. The implemented electronic registry has proven its effectiveness for monitoring morbidity, planning medical care and conducting scientific research, which determines the prospects for its further development to optimize the system of endocrinological care in the region.

Primary aldosteronism (PA) is the most common curable cause of secondary hypertension and an independent risk factor for chronic kidney disease (CKD). This review focuses on the pathophysiological mechanisms of aldosterone-induced renal injury, including mineralocorticoid receptor activation, nongenomic signaling via GPER, oxidative stress, and the upregulation of profibrotic and inflammatory mediators such as TGF-β1, NF-κB, and NLRP3. Chronic aldosterone excess leads to podocyte injury, microvascular dysfunction, and interstitial fibrosis, resulting in decreased glomerular filtration rate and CKD progression.

Genetic mutations (KCNJ5, ATP1A1, CACNA1D) and tubular stress biomarkers (L-FABP, KIM-1, microalbuminuria) are discussed as key factors of early nephron injury. Comparative clinical data show that adrenalectomy provides superior nephroprotection compared to pharmacological blockade, while long-term therapy with mineralocorticoid receptor antagonists requires careful renal monitoring. Emerging therapeutic strategies, including nonsteroidal MR antagonists and aldosterone synthase inhibitors (baxdrostat), offer new prospects for targeted nephroprotection.

By integrating molecular and clinical evidence, this review highlights the central role of aldosterone in renal pathology and emphasizes early detection and personalized treatment approaches to prevent CKD progression in patients with PA.

This descriptive clinical case series analyzes five cases of destructive thyrotoxicosis associated with Hashimoto’s thyroiditis, historically referred to as hashitoxicosis, initially misdiagnosed as Graves’ disease, highlighting a persistent diagnostic challenge in autoimmune thyroid disorders. The series includes four published cases reported between 2000 and 2025 and one unpublished case contributed by the authors. The cohort comprised three females and two males, with a mean age of 55.4 years (range: 21–69). Clinical presentations were heterogeneous, most commonly fatigue (80%), palpitations (60%), and weight changes (40%), while two patients exhibited no overt hyperthyroid symptoms.

Biochemical evaluation demonstrated suppressed thyroid-stimulating hormone (TSH) levels in all cases (range: <0.000–0.13 µIU/mL), elevated anti-thyroid peroxidase (anti-TPO) antibodies in 80% (range: 41–>1,000 IU/mL), and initially negative thyroid-stimulating hormone receptor antibodies (TRAb/TSI) in 60% of patients. Seroconversion to positive TRAb/TSI was observed in two cases during follow-up, suggesting autoimmune overlap rather than definitive disease transition. Imaging findings, including thyroid ultrasonography and radioiodine uptake (RAI) studies, consistently favored destructive thyroiditis over stimulatory hyperthyroidism, with heterogeneous echotexture observed in 75% of assessed cases and low or normal RAI uptake in all evaluated patients.

Misdiagnosis occurred in 80% of cases, predominantly due to reliance on suppressed TSH levels without TRAb confirmation, resulting in inappropriate antithyroid drug administration in 80% and accelerated hypothyroidism in 60%. Immunopathological interpretation based on existing literature supports a predominantly Th1-mediated destructive process, in contrast to the Th2-driven antibody-mediated stimulation characteristic of Graves’ disease, with rare Th1-to-Th2 immune shifts reported. Clinical outcomes ranged from spontaneous resolution to surgical intervention.

This case series underscores the importance of mandatory TRAb testing, adherence to American and European Thyroid Association guidelines, and early specialist referral to reduce iatrogenic harm and improve diagnostic precision in autoimmune thyroid disease.

On December 3, 2025, a meeting of the expert working group was held in Moscow. The discussion focused on the safety and personalized use of tirzepatide (Tirzetta®) and semaglutide (Velgia® eco) in patients with overweight and obesity. Following the meeting, a consensus position was developed on the optimal use of incretin receptor agonists in real-world clinical practice.

Gluconeogenesis, a dual-purpose pathway in type 2 diabetes mellitus (T2DM), not only synthesizes glucose but also clears metabolic waste via the Cori cycle (lactate recycling through LDH, PC, PEPCK) and Alanine cycle (nitrogen disposal via ALT, GDH, urea cycle), preventing acidosis, ROS accumulation, and ammonia toxicity. Metformin, the cornerstone T2DM therapy, inhibits gluconeogenesis by targeting mitochondrial complex I, elevating AMP/ATP ratios, and activating AMPK-PKCι/λ signaling to repress CREB-CRTC2-driven PEPCK/G6Pase expression, disrupting these cycles. This leads to lactate, pyruvate, and ammonia buildup, triggering pro-inflammatory cascades: HIF-1α stabilization induces IL-6/VEGF, ROS from pyruvate excess activates NF-κB for TNF-α, and ammonia primes NLRP3 inflammasome for IL-1β/IL-18 release, fostering chronic inflammation. Multisystem consequences include musculoskeletal fatigue from ATP deficits, cognitive fog via neuroinflammation, atherosclerosis from endothelial dysfunction, hepatic fibrosis from urea cycle stress, and immune inflammaging impairing macrophage function. Clinical evidence reveals short-term anti-inflammatory benefits (reduced IL-6, CRP) via AMPK and microbiota effects, contrasted by long-term risks like lactic acidosis and neurodegeneration in renal-impaired or elderly patients. This review integrates physiological roles, molecular mechanisms, inflammatory pathways, systemic impacts, and clinical findings, highlighting metformin’s dual-edged profile glycemic efficacy versus “inflammatory debt.” Researchers are urged to explore precision interventions, such as antioxidants or biomarker-guided dosing, to optimize metformin’s pleiotropic potential in T2DM and inflammaging-related disorders, redefining therapeutic paradigms.

BACKGROUND. Vitamin D deficiency is one of the most common endocrine disorders and plays a significant role in the pathogenesis of carbohydrate metabolism disturbances. Low serum 25(OH)D levels are associated with the development of insulin resistance, metabolic syndrome, prediabetes, and type 2 diabetes mellitus (T2DM). However, data on the prevalence of vitamin D deficiency and its age-related characteristics in the population of Uzbekistan remain limited.

OBJECTIVE. To investigate the prevalence of vitamin D deficiency in individuals with prediabetes and newly diagnosed T2DM based on screening data from the city of Andijan and the Markhamat district of the Andijan region, Uzbekistan.

MATERIALS AND METHODS. A total of 3,400 individuals over 40 years of age were screened (1,800 in Markhamat district, 1,600 in Andijan city) using the FINDRISC questionnaire. Serum 25(OH)D levels, carbohydrate and lipid metabolism parameters, and HOMA-IR index were assessed in 205 subjects with prediabetes, 102 patients with newly diagnosed T2DM, and 60 controls. Prediabetes and T2DM were diagnosed according to WHO criteria.

RESULTS. Mean vitamin D levels were significantly lower in patients with prediabetes and T2DM compared to the control group (p<0.05). The most severe deficiency was observed in patients with T2DM, especially among women and individuals aged 45–59 and 60–74 years. In Andijan city, vitamin D deficiency was detected in 100% of T2DM patients, while in Markhamat district the prevalence reached 40.3%.

CONCLUSIONS. Vitamin D deficiency is highly prevalent among patients with prediabetes and T2DM, with severity increasing with age and more pronounced in women. These findings highlight the need for routine monitoring of serum 25(OH)D and preventive strategies in high-risk groups.

Glucagon-like peptide-1 receptor agonists (GLP-1RAs) like semaglutide have transformed type 2 diabetes mellitus (T2DM) management, yet emerging concerns highlight potential risks of accelerated sarcopenia and subsequent metabolic disruptions. This case-driven hypothesis explores a 53-year-old male with T2DM diagnosed in 2014, who experienced progressive glycemic failure despite standard therapies, including metformin, glipizide, sitagliptin, and empagliflozin. Transition to dulaglutide 1.5 mg for 1.5 years followed by semaglutide (titrated from 0.25 to 1 mg weekly starting September 2024) resulted in weight loss from 84 kg to 70 kg by September 2025, accompanied by sarcopenic symptoms (muscle weakness, reduced mobility) and refractory hyperglycemia (fasting glucose 300 mg/dL, HbA1c 9%), persisting post-discontinuation on September 1, 2025, despite metformin and empagliflozin. We posit that semaglutide may precipitate acute sarcopenia via unexpected GLP-1R-mTOR-satellite cells axis crosstalk, disrupting AMPK-mTOR balance to suppress anabolic mTORC1/IGF-1 signaling (potentially by 25-35%) while enhancing catabolic FOXO/ubiquitin-proteasome and excessive autophagy pathways. This could extend to myokine reprogramming (elevated myostatin/GDF15, reduced irisin/IL-15), glucagon/α-cell compensation inducing hyperglucagonemia (15-25% rise), microbiome-bile acid shifts fostering low-grade inflammation (IL-6/TNF-α upregulation by 10-15%), mitochondrial mass reduction (20-25% via AMPK), and NMJ disassembly, collectively impairing muscle as the primary glucose sink (reducing GLUT4-mediated uptake by 35-45%) and initiating a «muscle-glucose feedback loop» with hepatic gluconeogenesis amplification, yielding treatment-resistant hyperglycemia.

Supporting evidence from cohorts (e.g., 24-month study showing ASMI/grip strength declines in 432 patients), longitudinal analyses (NMJ degradation with CAF22/NfL elevations in 141 men), secondary trials (9.3% psoas volume loss in 51 MASLD cases), and case reports (fatigue in a 74-year-old, rhabdomyolysis in a 47-year-old) aligns with this framework, as does in vitro data linking GLP-1 excess to kinesin-1/GLUT4 inhibition and ATP depletion (20-30%). This novel hypothesis underscores sarcopenia’s role in GLP-1RA-induced metabolic paradoxes, urging prospective studies on muscle-preserving interventions like resistance training or GLP-1R modulators to refine T2DM paradigms and inspire multidisciplinary research into endocrine-muscle interactions.

BACKGROUND: Differentiated thyroid carcinoma (DTC) in children is a rare malignancy characterized by a high propensity for regional and distant metastases yet generally associated with a favorable long-term prognosis. Radioiodine-refractory (RAIR) disease represents a distinct clinical challenge, accounting for approximately 10–30% of pediatric DTC cases, and warrants comprehensive investigation of its clinical course, prognostic factors, and therapeutic options. This study aimed to perform an integrated assessment of treatment outcomes in children undergoing combined therapy for DTC (surgery and radioiodine therapy, RAI), with a particular focus on advanced and RAIR disease.

MATERIALS AND METHODS: We retrospectively analyzed medical records of 278 patients aged 5–18 years who underwent primary surgical treatment between 2008 and 2022, followed by one or more courses of RAI at the Endocrinology Research Centre (Moscow, Russia) from December 2015 to March 2024. The study included patients with advanced disease (high risk of recurrence at diagnosis) fulfilling at least one RAIR criterion, with a median follow-up of 48.0 months [21.5; 62.0].

RESULTS: Among 278 patients, 39 (14%) were diagnosed with advanced disease. Of these, 4 achieved remissions, 29 had stable disease, and 6 experienced biochemical and/or structural progression. Progression-free survival in the RAIR cohort was 85%, while the 5-year overall survival reached 100%.

CONCLUSION: Based on study findings, we propose a novel classification system integrating both the baseline ability of metastases to accumulate ¹³¹I and the dynamic response to RAI (progression vs. stabilization). This framework is designed to optimize treatment and follow-up algorithms. The management of RAIR pediatric DTC should remain balanced: avoiding overtreatment in stable disease, while ensuring timely initiation of modern systemic therapies in patients with risk factors for progression.

Microcephalic osteodysplastic primary dwarfism type II (MOPDII) is a form of primordial nanism characterized by extreme short stature, microcephaly, specific phenotype, maxillofacial dysmorphisms, skeletal dysplasia, disorders of carbohydrate metabolism, and neurovascular abnormalities. This article describes a patient with a Seckel syndrome phenotype presenting with left internal carotid artery aneurysms with intracerebral hemorrhages, thrombocytosis, arterial hypertension, and diabetes mellitus due to insulin resistance confirmed by a low Matsuda index. Target carbohydrate metabolism values were achieved on metformin therapy. Clinical exome sequencing revealed two rare heterozygous variants in the PCNT gene: c.6220C>T (p.Gln2074*) and c.4564-12T>A. Comparison of the results of the molecular genetic study and the patient’s phenotype allowed us to verify the diagnosis of MOPDII. Hypergonadotropic hypogonadism was described for the first time in this syndrome.

The clinical practice guidelines for congenital adrenal hyperplasia (CAH) in children clearly and systematically present the key information on the epidemiology, etiology, pathogenesis, and diagnostic methods for all forms of the disease. Protocols for glucocorticoid and mineralocorticoid replacement therapy, as well as follow-up regimens for patients in different age groups, are provided. These clinical guidelines were developed and approved by the expert community of pediatric endocrinologists from the Russian Association of Endocrinologists and endorsed by the council of the Russian Federation Ministry of Health. The guidelines are based on systematic reviews, meta-analyses, original articles, and scientific studies on this pathology conducted in the Russian Federation and other countries. This article provides updated author comments and clarifications on the most critical aspects of the diagnosis and treatment of congenital adrenal hyperplasia in childhood.